Sex and muscle structural lipids in obese subjects - an impact on insulin action?

BACKGROUND: Long-chain polyunsaturated fatty acid (LCPUFA) especially the n-3-FA of skeletal muscle phospholipids may facilitate insulin action, whereas saturated and trans-FA act oppositely. Community studies show that non-diabetic weight matched obese men and women display similar insulin resistance, despite the fact that an android fat distribution is detrimental to insulin action. The increased extramyocellular fat mass of obese women may act in a paracrine manner such that its release of free FA and cytokines may hamper in situ desaturation and elongation of FA in skeletal muscle phospholipids. MATERIAL AND METHODS: To test the hypothesis that obese women may display an inferior FA composition compared to obese men, the FA composition of skeletal muscle phospholipids was determined in vastus lateralis biopsies obtained from 12 non-diabetic obese women with a typical gynoid fat distribution, nine non-diabetic obese men with a typical android fat distribution and 12 (seven females) lean age matched healthy controls (body mass index 34.6 +/- 1.0 kg m(-2), 36.5 +/- 1.2 and 22.5 +/- 0.5; age 47 +/- 2 years, 51 +/- 3 and 49 +/- 2). RESULTS: Obese women displayed decreased LCPUFA n-3 and ratio of n-3/n-6 PUFA, whereas trans-FA and palmitic-FA (C16 : 0) were increased compared to obese men and controls (all Ps < 0.05). Plasma high-density lipoprotein cholesterol (HDL-C), triglycerides and a marker of insulin sensitivity were similar between obese women and men but impaired compared to controls (Ps < 0.05). CONCLUSIONS: The data support the hypothesis that insulin resistant non-diabetic obese men display a more optimal skeletal muscle phospholipid FA composition than their female counterparts, which may be a mechanism to compensate the detrimental effect on insulin action of an android fat distribution.

Fatty acid profiles of brain phospholipid subclasses of rats fed n - 3 polyunsaturated fatty acids of marine or vegetable origin. A two generation study.

The effects of dietary n - 3 polyunsaturated fatty acids (PUFA) on fatty acid profiles of rat brain phospholipid subclasses as well as on heart phosphatidylethanolamine through two generations were examined: Three groups of rats were fed 20 weight% fat diets in which approx. 30% of the fatty acids were polyunsaturated, either 17% linoleic acid + 13% C20(-) + C22 polyunsaturates from fish oil or 17% linoleic + 13% alpha-linolenic acid from linseed oil or 30% linoleic acid. The rats of the two generations were killed as adults at 18 weeks of age. The results demonstrated that fish oil was a better source than alpha-linolenic acid for incorporation of n - 3 PUFA into the examined phospholipids. This was seen both in brain and heart tissue and in both generations of rats. In the brain phosphatidylethanolamine (PE) and phosphatidylserine (PS) similar fatty acid profiles were found in 1st and 2nd generation, but fish oil was more efficient than 18:3(n - 3) in increasing the levels of 22:6(n - 3), 20:5(n - 3), 22:5(n - 3) and reducing 20:4(n - 6) and 22:5(n - 6). Fatty acid profiles of phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2) were affected by dietary fats. In PIP and PIP2 of 2nd generation rats 20:4(n - 6) was reduced from 36 to 29% following fish oil intake, whereas alpha-linolenic acid had no effects. The cholesterol/phospholipid ratio was not affected in the brain, neither was the degree of unsaturation of the phospholipids. In heart PE the highest levels of 20:5(n - 3)(2%) and 22:6(n - 3) (36%) were observed following fish oil intake. However, in rats fed alpha-linolenic acid a considerable increase in the level of 22:6(n - 3) was observed from the 1st (21%) to the 2nd generation (26%).

Correlation between level of (n - 3) polyunsaturated fatty acids in brain phospholipids and learning ability in rats. A multiple generation study.

The effects of dietary n - 3 polyunsaturated fatty acids (PUFAs) on major brain phospholipids were examined in the rat throughout four generations. Dietary fats were: a seal oil (22:6(n - 3) located mainly in the sn-1/3-position of the TG); a fish oil (22:6(n - 3) located mainly in the sn-2 position of the TG); or a vegetable oil containing 18:3(n - 3). The effect of the TG structure of the dietary fat and chain length of n - 3 PUFA on assimilation in the brain was compared with chow fed rats. The rats fed marine fats had significantly higher levels of long-chain n - 3 PUFAs in brain PE and PS, compared to the vegetable oil and chow fed rats, but no effects of TG structure of dietary fat were observed. Dietary 18:3(n - 3) raised the amount of 22:6(n - 3) compared to the control group, but not to the levels of the marine groups that received preformed 22:6(n - 3). Fish oil fed rats had higher levels of 20:5(n - 3) and 22:5(n - 3) compared with the seal oil fed rats, whereas 22:6(n - 3) were similar. Only minor changes in PI, PIP, and PIP2 were found. The fourth generation was tested for spatial learning ability in a Morris water maze. The experimental groups had similar learning abilities, which were increased compared to the control group.

Lymphatic absorption of n - 3 polyunsaturated fatty acids from marine oils with different intramolecular fatty acid distributions.

Male Wistar rats were given 0.5 ml of either fish oil or seal oil intragastrically. The intramolecular fatty acid distributions of the triacylglycerols administered were determined by non-specific Grignard degradation followed by isolation and analysis of the 2-monoacylglycerols. The n - 3 polyunsaturated fatty acids (PUFAs), especially eicosapentaenoic acid (20:5(n - 3)) and docosahexaenoic acid (22:6(n - 3)), were located in outer positions (sn-1/3) in the seal oil triacylglycerols whereas the sn-2 position of fish oil triacylglycerols was enriched in 20:5(n - 3) and 22:6(n - 3). The mesenteric lymph was collected over the following 24 h and the absorption patterns of n-3 PUFAs were determined. In the lymph, the n - 3 fatty acids characteristic of the marine oils rapidly increased both with regard to mole percentage and transport (micrograms/min). There were, however, no overall significant differences in the absorption patterns over a 24 h period. The ratio between mole percentage in the oil and mole percentage in the lymph calculated at the steady-state period was significantly greater for both 20:5(n - 3) and 22:6(n - 3) following fish oil administration compared with seal oil. Initially, the recovery of n - 3 PUFAs as a percentage of the total amount transported over the experimental period was higher following injection of fish oil than seal oil but seal oil resulted in greater recovery in the last two fractions at 8 and 24 h post injection, respectively. This indicated that n - 3 PUFAs from fish oil may have been better absorbed in the initial period of digestion but overall the structure of dietary triacylglycerols had negligible effects on the assimilation of n - 3 PUFAs when these were administered as native marine oils.

Essential fatty acid deficiency in patients receiving home parenteral nutrition.

Home parenteral nutrition (HPN), initiated in patients with severe malabsorption or decreased oral intake, may exhaust stores of essential fatty acids and cause clinical manifestations, mainly dermatitis. Plasma fatty acid profiles were measured by gas-liquid chromatography in 37 healthy control subjects and 56 patients receiving HPN. The concentration (% by wt of total fatty acids) of 18:2n-6 was 22.8% and 11.4% (P < 0.001), whereas 18:3n-3 was 0.2% and 0.1% (P < 0.01) in control subjects and patients, respectively. Reduced small bowel length was associated with aggravated biochemical signs of essential fatty acid deficiency (EFAD). The effect of parenteral lipid on plasma phospholipids was evaluated in subgroups of patients. In patients with > 200 cm of remaining small intestine, those receiving parenteral lipids had only minor changes in the fatty acids of plasma phospholipids compared with patients not receiving parenteral lipids. In patients with < 100 cm of remaining small intestine, those receiving parenteral lipids had increased concentrations of total n-6 fatty acids; however, these did not reach the concentrations in control subjects. No differences were seen in n-3 fatty acids. Twenty-five of the 56 patients receiving HPN reported skin problems. No differences were found in plasma phospholipid fatty acids, Holman index, or the supply of parenteral lipids between patients with and without skin problems. Patients receiving HPN had biochemical signs of EFAD. Parenteral lipids did not increase the concentration of essential fatty acids to values comparable with those of control subjects, but 500 mL 20% Intralipid once a week was sufficient to prevent an increase in the Holman index above 0.2.

Differences in essential fatty acid requirements by enteral and parenteral routes of administration in patients with fat malabsorption.

BACKGROUND: Essential fatty acid (EFA) requirements of patients receiving home parenteral nutrition (HPN) are uncertain. OBJECTIVE: The objective was to evaluate the influence of the route of administration (enteral compared with parenteral) on plasma phospholipid EFA concentrations. DESIGN: Intestinal absorption, parenteral supplement of EFAs, and plasma phospholipid EFA concentrations were investigated in balance studies in 4 groups (A, B, C, and D) of 10 patients with short-bowel syndrome and a fecal loss of >2000 kJ/d. Groups A (fat malabsorption <50%) and B (fat malabsorption >50%) did not receive HPN, whereas group C received HPN containing lipids (7.5 and 1.2 g/d linoleic and linolenic acids, respectively) and group D received fat-free HPN. RESULTS: Intestinal absorption of linoleic and linolenic acids was 8.9 and 1.3 g/d and 2. 6 and 0.4 g/d in groups A and B, respectively, whereas EFA absorption was negligible in groups C and D. Thus, intestinal absorption of EFAs in group A corresponded to parenteral EFA supplements in group C, whereas group D was almost totally deprived of EFAs. The median plasma phospholipid concentration of linoleic acid decreased by 21.9%, >16.3%, >13.8%, 11.0%, and >7.7% and linolenic acid by 0.3%, 0.2%, 0.2%, >0.2%, and 0.1%, respectively, in 10 healthy control subjects and groups A, B, C, and D (P < 0.001). CONCLUSIONS: Intestinally absorbed EFAs maintained plasma EFA status better than did an equal quantity of parenterally supplied EFAs. Intravenous requirements of EFAs in patients with negligible absorption of EFAs are probably higher than the amounts recommended to patients with preserved intestinal absorption of EFAs.

Intestinal absorption and lymphatic transport of eicosapentaenoic (EPA), docosahexaenoic (DHA), and decanoic acids: dependence on intramolecular triacylglycerol structure.

We compared the absorption of eicosapentaenoic (EPA, 20:5n-3), docosahexaenoic (DHA, 22:6n-3), and decanoic acids in mesenteric lymph duct-cannulated rats following intragastric administration of two oils with different intramolecular triacylglycerol structures. One oil had a specific triacylglycerol structure with EPA and DHA located in the sn-2 position and decanoic acid in the sn-1 and sn-3 positions (specific M-n3-M) whereas the other oil had a random fatty acid distribution (random M-n3-M). The mol% (mol/100 mol total fatty acids) of fatty acids in the two oils was similar, with approximately 66 mol% of decanoic acid and 22 mol% of EPA and DHA. The lymphatic transport (microgram/min) of EPA and DHA as well as the mol% in the total lymph lipids were significantly (both P < 0.01) increased following intragastric administration of specific M-n3-M compared with random M-n3-M. The mol% of decanoic acid in the total lymph lipids was significantly (P < 0.01) higher after random M-n3-M compared with specific M-n3-M but the transport (microgram/min) of decanoic acid was not significantly different. We conclude that under our experimental conditions specific M-n3-M with EPA and DHA predominantly in the sn-2 position of the triacylglycerols was a more readily absorbed source of EPA and DHA and in this context should be investigated further for the potential use in clinical nutrition.

Essential fatty acid deficiency in patients with severe fat malabsorption.

Essential fatty acid deficiency is commonly described in patients receiving parenteral nutrition, but the occurrence in patients with severe fat malabsorption not receiving parenteral nutrition is uncertain. One hundred twelve patients were grouped according to their degree of fat malabsorption: group 1, < 10% (n = 52); group 2, 10-25% (n = 21); group 3, 25-50% (n = 24); and group 4, > 50% (n = 15). Fecal fat was measured by the method of Van de Kamer the last 2 of 5 d of a 75-g fat diet. Serum fatty acids in the phospholipid fraction were measured by gas-liquid chromatography after separation by thin-layer chromatography and expressed as a percentage of total fatty acids. The concentration of linoleic acid in groups 1, 2, 3, and 4 was 21.7%, 19.4%, 16.4%, and 13.4% respectively (P < 0.001). The concentration of linolenic acid in groups 1, 2, 3, and 4 was 0.4%, 0.4%, 0.3% and 0.3%, respectively (P = 0.017). Evidence of essential fatty acid deficiency, defined as a serum concentration of linoleic acid less than the lower limit if the 95% CI in patients without fat malabsorption (group 1), was 5% (1/21), 38% (9/24), and 67% (10/15) in groups 2, 3, and 4, respectively. A considerable proportion of patients with gastrointestinal diseases resulting in malabsorption of > 25-50% of dietary fat intake and not treated with parenteral nutrition have biochemical signs of essential fatty acid deficiency. The clinical effect of these changes are yet to be elucidated.

Effect of fish-oil-enriched margarine on plasma lipids, low-density-lipoprotein particle composition, size, and susceptibility to oxidation.

We investigated the effect of incorporating n-3 polyunsaturated fatty acids (PUFAs) into the diet on the lipid-class composition of LDLs, their size, and their susceptibility to oxidation. Forty-seven healthy volunteers incorporated 30 g sunflower-oil (SO) margarine/d into their habitual diet during a 3-wk run-in period and then used either SO or a fish-oil-enriched sunflower oil (FO) margarine for the following 4 wk. Plasma concentrations of total cholesterol, triacylglycerols, HDL cholesterol, LDL cholesterol, and apolipoproteins A-I and B did not differ significantly between the groups during intervention. The FO margarine increased the concentration of n-3 very-long-chain PUFAs in the LDL particles, showing 93% (P < or = 0.0001), 8% (P = 0.05), and 35% (P = < 0.0001) increases in eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid, respectively, in the FO group compared with 3%, 7%, and 7%, respectively, in the SO group during the intervention. The cholesterol content of the LDL particles increased in the FO group [total cholesterol: 6% (P = 0.008); cholesterol ester: 12% (P = 0.014)], although it was not significantly different from that in the control group, whereas the other lipid classes and the size of the LDL particles remained unchanged in both groups. A reduction in the alpha-tocopherol content in LDL (6%, P = 0.005) was observed in the FO group. Ex vivo oxidation of LDL induced with Cu2+ showed a significantly reduced lag time (from 91 to 86 min, P = 0.003) and lower maximum rate of oxidation (from 10.5 to 10.2 nmol x mg(-1) x min(-1), P = 0.003) after intake of the FO margarine. The results indicate that consumption of the FO compared with the SO margarine had no effect on LDL size and lipid composition and led to minor changes in LDL a-tocopherol content and oxidation resistance.

Deficiencies of essential fatty acids, vitamin A and E and changes in plasma lipoproteins in patients with reduced fat absorption or intestinal failure.

OBJECTIVE: Deficiencies of essential fatty acids (EFA), vitamin A (retinol) and vitamin E (alpha- and gamma-tocopherol) were studied in non-HPN patients with different degrees of fat malabsorption (managing without home parenteral nutrition (HPN)), and in HPN-patients receiving HPN with and without parenteral lipids. DESIGN AND SUBJECTS: Phospholipid fatty acids (including EFA), cholesterol, retinol, alpha- and gamma-tocopherol in plasma and the intestinal absorption of fatty acids and energy (balance-studies) were measured in 40 non-HPN patients, 44 HPN patients and 35 controls. Subgroups were non-HPN patients with fat:total energy absorption ratios >25% (A), between 15 and 25% (B), and <15% (C), and HPN patients receiving (D) and not receiving parenteral lipids (E). RESULTS: Intestinal absorption of the EFA linoleic acid was 8.2, 4.4, 3.8, 0.5 and 0.5 g/day and corresponding plasma concentrations were 17.3%, 15.5%, 13.1%, 12.1% and 8.9% in groups A-E, respectively (P<0.001). Deficiencies in EFA, defined as a Holman index >0.2 (20:3n-9/20:4n-6 ratio), were confined to 42% of the patients in group E. Plasma cholesterol was decreased in groups B-E. Plasma retinol was reduced (below the lower 2.5% confidence interval of controls) in 7% of non-HPN patients and in 20% of HPN patients. Plasma alpha-tocopherol was reduced in 64% of patients from groups B-E. Plasma gamma-tocopherol was decreased in 33% of the patients, except in HPN-patients receiving parenteral lipids. CONCLUSIONS: Plasma linoleic acid may decrease considerably (from 26% to 8-10%) as fat absorption decreases before secondary signs of essential fatty acid deficiencies occur (an increase in 20:3n-9 and the Holman index). In this study this was confined to patients on lipid-free HPN. Vitamin A deficiencies were mainly seen in HPN patients. Vitamin E deficiencies were common in both HPN and non-HPN patients, but administration of parenteral lipids normalized plasma gamma-tocopherol. European Journal of Clinical Nutrition (2000) 54, 632-642.

Comparison of total oral bioavailability and the lymphatic transport of halofantrine from three different unsaturated triglycerides in lymph-cannulated conscious rats.

The lymphatic transport and the portal absorption of the lipophilic drug halofantrine were investigated in a conscious rat model. The rats were dosed with 0.1 g with triolein, trilinolein or trilinolenin containing 2 mg halofantrine. Following oral administration of the triglycerides, the mesenteric lymph and plasma samples were collected. The lymphatic transport for halofantrine was 11.1+/-1.2 after administration of trilinolein, 9.0+/-3.5 for trilinolenin and 8.6+/-2.2 for triolein and the total amount of halofantrine transported in the lymph was linear proportional with the amount of triglyceride in the lymph. The absorption of halofantrine directly into the blood showed a trend towards a higher AUC for trilinolien and trilinolenin compared to triolein, but no statistical difference could be found. The statistically analysis of the mean total bioavailability therefore shows that the absorption of halofantrine was largely independent on triglyceride unsaturation.

Synthesis of structured triacylglycerols containing caproic acid by lipase-catalyzed acidolysis: optimization by response surface methodology.

Production in a batch reactor with a solvent-free system of structured triacylglycerols containing short-chain fatty acids by Lipozyme RM IM-catalyzed acidolysis between rapeseed oil and caproic acid was optimized using response surface methodology (RSM). Reaction time (t(r)), substrate ratio (S(r)), enzyme load (E(l), based on substrate), water content (W(c), based on enzyme), and reaction temperature (T(e)), the five most important parameters for the reaction, were chosen for the optimization. The range of each parameter was selected as follows: t(r) = 5-17 h; E(l) = 6-14 wt %; T(e) = 45-65 degrees C; S(r) = 2-6 mol/mol; and W(c) = 2-12 wt %. The biocatalyst was Lipozyme RM IM, in which Rhizomucor miehei lipase is immobilized on a resin. The incorporation of caproic acid into rapeseed oil was the main monitoring response. In addition, the contents of mono-incorporated structured triacylglycerols and di-incorporated structured triacylglycerols were also evaluated. The optimal reaction conditions for the incorporation of caproic acid and the content of di-incorporated structured triacylglycerols were as follows: t(r) = 17 h; S(r) = 5; E(l) = 14 wt %; W(c) = 10 wt %; T(e) = 65 degrees C. At these conditions, products with 55 mol % incorporation of caproic acid and 55 mol % di-incorporated structured triacylglycerols were obtained.

Incorporation of cis-octadecenoic acids into the rat liver mitochondrial membrane phospholipids and adipose tissue triglycerides.

The incorporation of the dietary cis 18:1(n-12) and cis 18:1(n-10) into liver mitochondrial membrane phospholipids and adipose tissue triglycerides was studied in 4 groups of rats fed diets containing 10 weight percent (wt %) of fat with the following contents of octadecenoic acids: 50% cis 18:1(n-12) + 9% cis 18:1(n-9); 25% cis 18:1(n-12) + 32% cis 18:1(n-9); 50% cis 18:1(n-10) + 10% cis 18:1(n-9); or 54% cis 18:1(n-9). Dietary linoleic acid was 3 wt % in all 4 groups. In the mitochondrial membranes, the isomeric octadecenoic acids were primarily incorporated into the 1-position of phosphatidylcholines and phosphatidylethanolamines at the expense of saturated fatty acids. The maximal incorporations observed in the 1-position of phosphatidylethanolamines were 4.8% 18:1(n-12) and 8.9% 18:1(n-10). No effects on the contents of polyunsaturated fatty acids in the phospholipids were seen. In the adipose tissue, the isomeric octadecenoic acids were incorporated at a level of 13% cis 18:1(n-12) or 23% cis 18:1(n-10), paralleled by a reduction in the content of oleic acid.

Incorporation of cis- and trans-octadecenoic acids into the membranes of rat liver mitochondria.

The incorporation of dietary isomeric fatty acids into the membranes of liver mitochondria was investigated. Three groups of rats were fed diets containing 3% sunflower seed oil plus 15%, 20%, or 25% partially hydrogenated arachis oil. A fourth group was fed 25% partially hydrogenated arachis oil, but no sunflower seed oil. All diets were given for 3, 6, or 10 weeks. After 10 weeks, the content of trans fatty acids in the lipids of the mitochondrial membranes was 15--19% of the total fatty acids. The composition of the trans- and the cis-octadecenoic acids in the lipids of the mitochondrial membranes was similar for all groups supplemented with sunflower seed oil (SO), irrespective of time and dietary level of partially hydrogenated arachis oil (HAO). The cis 18:1 (n-8), which was a major isomer of the partially hydrogenated arachis oil, was almost excluded from the mitochondrial fatty acids. Likewise, the content of trans 18:1 (n-8) was considerably lower in the mitochondrial lipids than in the diet. On the contrary, the content of trans 18:1 (n-6) was higher in the mitochondrial lipids than in the diet. In the group fed without sunflower seed oil, isomers of linoleic acid and arachidonic acid were observed in the lipids of mitochondrial membranes.

Effects of dietary triacylglycerol structure on triacylglycerols of resultant chylomicrons from fish oil- and seal oil-fed rats.

We investigated the influence of the intramolecular fatty acid distribution of dietary triacyl-sn-glycerols (TAG) rich in n-3 polyunsaturated fatty acids (PUFA) on the structure of chylomicron TAG. Fish oil and seal oil, comparable in fatty acid compositions but with different contents of major n-3 PUFA esterified at the sn-2 position (20:5n-3, 46.6%, and 5.3%; 22:6n-3, 75.5%, and 3.8%, respectively), were fed to rats. Mesenteric lymph was collected and the chylomicrons were isolated by ultracentrifugation. The fatty acid composition of chylomicrons largely reflected the fatty acid composition of the oils administered. The intramolecular fatty acid distributions of the TAG fed were reflected in the chylomicron TAG as the fraction of the total contents observed in the sn-2 position of 20:5n-3 were 23.6 and 13.3%, and of 22:6n-3 were 30.6 and 5.4% for resultant chylomicrons following fish oil and seal oil administration, respectively. Thus, after seal oil administration, significant higher load of n-3 PUFA was esterified in the sn-1,3 positions of chylomicron TAG compared with fish oil administration (P < 0.05).

Early dietary intervention with structured triacylglycerols containing docosahexaenoic acid. Effect on brain, liver, and adipose tissue lipids.

Newborn rats were fed liquid diets containing 7 wt% fat in which 3.8% of the total fatty acids were 22:6n-3. The fats were either a specific structured oil with 22:6n-3 mostly located in the sn-2 position or a randomized oil with 22:6n-3 equally distributed in the triacylglycerol (TAG) molecules. The oils were manufactured by interesterification of fish oil TAG with free fatty acids from butterfat. The pups were tube-fed three times a day and stayed with their dams during the night. After 14 d they were fed solid diets containing the same oils for the next 7 d. A reference group stayed with the dams and received ordinary rat chow at weaning. In general no significant differences between the two dietary treatments were observed in the tissues examined except for adipose tissue. The levels of 22:6n-3 were significantly increased in brain phosphatidylcholines (PC) and phosphatidylserines (PS) of both experimental groups compared with the reference group after three weeks, whereas no differences were found in brain phosphatidylethanolamines (PE) and phosphatidylinositols (PI). In all groups and all phospholipids examined, the levels of 20:4n-6 generally decreased from 1 to 3 wk and were significantly lower in the experimental groups compared with the reference group at 3 wk except for PI. In liver, PC and PE 22:6n-3 remained constant in the experimental groups but decreased significantly in the reference group, whereas in liver PS 22:6n-3 increased in all groups, but reached significantly higher levels in the experimental groups than in the reference group. In adipose tissue, 22:6n-3 increased in the experimental groups during the study period, but decreased in the reference group, suggesting that a surplus of dietary 22:6n-3 was stored.

Dietary linoleic acid and the fatty acid profiles in rats fed partially hydrogenated marine oils.

The influence of the linoleic acid levels of diets containing partially hydrogenated marine oils (HMO) rich in isomeric 16:1, 18:1, 20:1 and 22:1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined. Five groups of rats were fed diets containing 20 wt % fat--16% HMO + 4% vegetable oils. In these diets, the linoleic acid contents varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents of trans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8% linoleic acid plus 32% trans fatty acids, mainly 18:1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and no trans fatty acids. As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n-6) polyunsaturated fatty acids (PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n-6) PUFA was reached that was not affected by further increase in dietary 18:2 (n-6) up to 14.5%. Compared with the HSOY- or PALM-fed rats, the plateau values of 20:4(n-6) were considerably lower and the contents of 18:2(n-6) higher in liver phosphatidylcholines (PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20:4(n-6), but decreased 22:5(n-6) compared with the PALM group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of different medium-chain fatty acids on intestinal absorption of structured triacylglycerols.

To study the effect of the chain length of medium-chain fatty acids on the intestinal absorption of long-chain fatty acids, we examined the lymphatic transport of fat following administration of five purified structured triacylglycerols (STAG) containing different medium-chain fatty acids in the sn-1,3 positions and long-chain fatty acids in the sn-2 position in a rat model. Significant amounts of medium-chain fatty acids were found in lymph samples after intragastric administration of 1,3-dioctanoyl-2-linoleyl-sn-glycerol (8:0/18:2/8:0), 1,3-didecanoyl-2-linoleyl-sn-glycerol, and 1,3-didodecanoyl-2-linoleyl-sn-glycerol. The accumulated lymphatic transport of medium-chain fatty acids increased with increasing carbon chain length. The recoveries of caprylic acid (8:0), capric acid (10:0), and lauric acid (12:0) were 7.3 +/- 0.9, 26.3 +/- 2.4, and 81.7 +/- 6.9%, respectively. No significant differences were observed for the maximal intestinal absorption of linoleic acid (18:2n-6) when the chain length of medium-chain fatty acids at the primary positions was varied, and the absorption of 18:2 and oleic acid (18:1) from 8:0/18:2/8:0 and 1,3-dioctanoyl-2-oleyl-sn-glycerol was similar. We conclude that the chain length of the medium-chain fatty acids in the primary positions of STAG does not affect the maximal intestinal absorption of long-chain fatty acids in the sn-2 position in the applied rat model, whereas the distribution of fatty acids between the lymphatics and the portal vein reflects the chain length of the fatty acids.

Influence of dietary linoleic acid and trans fatty acids on the fatty acid profile of cardiolipins in rats.

Cardiolipins (CL) have unique fatty acid profiles with generally high levels of polyunsaturated fatty acids, primarily 18:2n-6, and low levels of saturated fatty acids. In order to study the effect of dietary fatty acid isomers on the fatty acid composition of cardiolipins, rats were fed partially hydrogenated marine oils (HMO), rich in 16:1, 18:1, 20:1, and 22:1 isomeric fatty acids, supplemented with linoleic acid at levels ranging from 1.9% to 14.5% of total fat. Although the dietary fats contained 33% trans fatty acids, the levels of trans fatty acids in CL were below 2.5% in all organs. The fatty acid profiles of cardiolipins of liver, heart, kidney and testes showed different responses to dietary linoleic acid level. In liver, the contents of 18:2 reflected the dietary levels. In heart and kidney, the levels of 18:2 also paralleled increasing dietary levels, but in all groups fed HMO, levels of 18:2 were considerably higher than in the reference group fed palm oil. In testes, the 18:2 levels were unaffected by the dietary level of 18:2 and HMO.

Absorption by rats of tocopherols present in edible vegetable oils.

The absorption of tocopherols (alpha, gamma, and delta) and fatty acids from rapeseed (RO), soybean (SOO), and sunflower (SUO) oil, both from the natural oils and from the oils following moderate heating (180 degrees C for 15 min), was measured in lymph-cannulated rats. Oils were administered as emulsions through a gastrostomy tube, and lymph samples were collected for 24 h. The composition of tocopherols in oils and lymph fractions was measured by high-performance liquid chromatography, and fatty acids were measured by gas-liquid chromatography. The highest accumulated transport of alpha-tocopherol was observed after SUO administration, the lowest after SOO, with RO in between, corresponding to their relative contents (41.6 +/- 8.8, 32.7 +/- 5.0, and 24.9 +/- 4.3 microg at 24 h after administration of SUO, RO, and SOO, respectively). The calculated recoveries (in %) 24 h after oil administration were 21.4 +/- 4.5, 45.7 +/- 7.0, and 78.8 +/- 13.5 for SUO, RO, and SOO, respectively, suggesting that the absorption efficiency decreased when the alpha-tocopherol concentration increased. The recovery of alpha-tocopherol was higher than the recoveries of gamma- and delta-tocopherol, indicating that the different tocopherols were not absorbed to the same extent or with similar rates. No differences between unheated and heated oils were observed in the absorption of tocopherols, whereas heating led to lower absorption of fatty acids, thus showing no direct association between absorption of tocopherols and fatty acids.